Air Travel Hypoxemia vs the Hypoxia Inhalation Test in Passengers With COPD

Paul T. Kelly, MSc; Maureen P. Swanney, PhD; Leigh M. Seccombe, MSc; Chris Frampton, PhD; Matthew J. Peters, MD, PhD, FCCP; Lutz Beckert, MD, FCCP


CHEST. 2008;133(4):920-926. 

In This Article

Abstract and Introduction

Background: Limited data are available comparing air travel with the hypoxia inhalation test (HIT) in passengers with COPD. The aim of this study was to assess the predictive capability of the HIT to in-flight hypoxemia in passengers with COPD.
Methods: Thirteen passengers (seven female passengers) with COPD (mean [± SD], FEV1/FVC ratio, 44 ± 17%) volunteered for this study. Respiratory function tests were performed preflight. Pulse oximetry, cabin pressure, and dyspnea were recorded in flight. The HIT and a 6-min walk test were performed postflight. The in-flight oxygenation response was compared to the HIT results and respiratory function parameters.
Results: All subjects flew without the use of oxygen, and no adverse events were recorded in-flight (mean cabin altitude, 2,165 m; altitude range, 1,892 to 2,365 m). Air travel caused significant desaturation (mean preflight oxygen saturation, 95 ± 1%; mean in-flight oxygen saturation, 86 ± 4%), which was worsened by activity (nadir pulse oximetric saturation [SpO2], 78 ± 6%). The HIT caused mean desaturation that was comparable to that of air travel (84 ± 4%). The mean in-flight partial pressure of inspired oxygen (PIO2) was higher than the HIT PIO2 (113 ± 3 mm Hg vs 107 ± 1 mm Hg, respectively; p < 0.001). The HIT SpO2 showed the strongest correlation with in-flight SpO2 (r = 0.84; p < 0.001).
Conclusion: Significant in-flight desaturation can be expected in passengers with COPD. The HIT results compared favorably with the air travel data, with differences explainable by PIO2 and physical activity. The HIT is the best widely available laboratory test to predict in-flight hypoxemia.

Air travel causes significant hypobaric hypoxia in passengers with COPD.[1,2] Predicting the hypoxic response and related risk to air travel can be complicated. The Aerospace Medical Association guidelines[3] suggest that a stable preflight PaO2 of > 70 mm Hg is generally adequate for safe travel. Other suggested assessments include the ability to walk 50 yards at a normal pace or climbing a flight of stairs without becoming severely dyspneic.[3] A more sophisticated test for predicting air travel hypoxia, which has been recommended by the Aerospace Medical Association[3] and the British Thoracic Society,[4] is the hypoxia inhalation test (HIT). The HIT involves breathing a hypoxic gas mix for 20 min with the aim of predicting hypoxemia at the maximum allowable cabin pressure altitude of 2,438 m (8,000; feet).[5] At 2,438 m, the barometric pressure is approximately 565 mm Hg,[6] resulting in a partial pressure of inspired oxygen (PIO2) of 108 mm Hg.[7] To replicate the in-flight PIO2 at sea-level pressure, the HIT uses a fraction of inspired oxygen (FIO2) of 0.15 in a nitrogen balance. In-flight oxygen therapy is recommended if the HIT PaO2 falls to <50 to 55 mm Hg.[3,4]

The integrity of the HIT has been previously assessed.[8,9] Using a hypobaric chamber, Dillard et al[8] and Naughton et al[9] showed that hypobaric hypoxia at 2,438 m can be replicated by the HIT (FIO2, 0.151) in patients with COPD. This implies that the HIT can predict air-travel hypobaric hypoxia. However, both the HIT and chamber studies are performed in a stable environment, and may not fully represent the physical stresses and environmental variability of air travel, particularly over longer flight segments.

The HIT is considered to be the best available test for patient evaluation before air travel,[10] yet several authors[11,12] have questioned the HIT outcome recommendations. An 80% HIT failure rate (PaO2, < 55 mm Hg) has been reported in patients with COPD and interstitial lung disease, with 80% of subjects having flown asymptomatically in the last 5 years.[11] In a cohort of healthy passengers, we have reported[12] a normal HIT PaO2 range of 51 to 68 mm Hg, with three subjects falling to < 55 mm Hg. Participants whose PaO2 fell to < 55 mm Hg flew without the occurrence of an adverse event and had acceptable in-flight oxygen saturations. The HIT is designed to replicate hypoxemia at the lowest allowable cabin pressure (approximately 565 mm Hg). However, previous studies[12,13,14] have reported cabin pressures significantly > 565 mm Hg, indicating that the HIT may be more stressful than flight. Furthermore, a HIT and in-flight PaO2 of < 55 mm Hg may be a typical and tolerable response for passengers with chronic lung disease.

There have been a limited number of studies investigating the actual response to air travel in passengers with COPD. Significant hypoxemia has been reported during unpressurized flights (1,650 and 2,250 m)[1] and pressurized flights (1,829 m pressure equivalent)[2] in patients with COPD. Data comparing the HIT results using a recommended FIO2 of 0.15 and air travel in passengers with COPD are lacking. Furthermore, the current literature does not include continuous oximetry data on flights with various aircraft models and destinations. The aim of this study was to assess the capability of the HIT to predict in-flight hypoxemia in passengers with COPD.